14th Mar 2019
Recently, we were lucky enough to get some time with world expert in neuroscience and mental health, Professor Ed Bullmore. To ask him a few headline questions about the theme of his forthcoming free public lecture – “Inflamed Depression” – at the BNA2019 Festival of Neuroscience.
Professor Bullmore is a world expert in neuroscience and mental health.
He has been Professor of Psychiatry at the University of Cambridge since 1999, and in 2005, he also became Vice-President of Experimental Medicine at GlaxoSmithKline while maintaining his post at University of Cambridge.
Professor Bullmore's recently published book, "The Inflamed Mind", will form the basis of his 2019 Festival talk, discussing the new science on the link between depression and inflammation of the body and brain.
Q. Can you briefly explain the science behind the title of your lecture, ‘Inflamed Depression’?
Yes – the basic idea is that the immune system and the nervous system communicate with each other and that inflammatory activation of the immune system can have direct effects on the brain, mind and behaviour.
In particular, there’s growing evidence that inflammation, that’s the defensive response of the immune system to threats such as infection, can cause depression. My lecture – and my work – will focus on the how and why of the relationship between depression and inflammation and what that could mean for future scientific breakthroughs in the diagnosis and treatment of depression.
Q. How did you first make this important link between inflammation and depression?
Well, I should emphasise that other people were there well before me in seeing the causal links between inflammation and depression! The research that I will talk about and that features in the book is part of a growing international scientific interest in the connections between the nervous system and the immune system that dates back to the late 1980s.
At about the same time, coincidentally, while I was working as a young physician, I clearly remember treating a patient for rheumatoid arthritis, a severe inflammatory disease of the body, who was also suffering symptoms of depression. That was the moment when I first recognised that depression and inflammation can co-occur or coincide. When I reported this to a senior colleague, the consultant replied: “She’s depressed? Well you would be, wouldn’t you?” This dismissive but professionally respectable reaction, which I didn't challenge at the time, implied that the patient’s depression was caused by her knowledge that she had a painful, chronic, progressive disorder. Her mental state was a psychological reflection on her physical state.
The new science of neuro-immunology and immuno-psychiatry does now challenge that traditional, dualist interpretation by showing that there are many ways in which inflammation can directly cause changes in brain function and behaviour. So that patient I saw about 30 years ago, and many patients like her, could be depressed not just because “they would be, wouldn't they” - but - more simply in some ways - because depression, fatigue and other psychological symptoms can be directly caused by physical inflammation.
Q. So, what does this mean in terms of how we might approach depression in future?
Depression is one of the single biggest causes of disability worldwide. And yet the treatment for it hasn’t changed much in the last three decades. Currently, if you have physical symptoms along with symptoms of depression, your mind and body will be treated separately, by different hospital departments. I think this needs to change. The body and mind are much more integrated than our relatively segregated professional training paths and service delivery models for physical and mental healthcare. I would like to see a more joined-up approach to how we help patients with depressive symptoms in the context of inflammatory disease or low grade inflammation.
Q. By making these links, how might this change future treatments?
As confidence builds that inflammation can cause depression, by biologically defined mechanisms, then this also opens out the possibility that we could develop new treatments for depression that worked by reducing inflammation. I am very interested in this future scenario. I hope that we will see new anti-inflammatory interventions, including but not exclusively drugs, being developed for treatment of depressive symptoms in patients with blood test or biomarker evidence for inflammation.
This won’t be a panacea. I don't think inflammation causes all depression or that anti-inflammatory drugs will work for everyone with depression. That “one size fits all” approach is a limitation of where we are at the moment. The future, I hope, will take a more personalised approach, using anti-inflammatory interventions more precisely to target inflammation in those patients where it is likely to be a causal factor.
Professor Bullmore will be speaking at BNA2019 Festival of Neuroscience in Dublin, 14-17 April. You can book a free place on his lecture here. Plus, find out more about the Festival here.
For more information on Professor Bullmore’s book, “The Inflamed Mind”, click here.
